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Researchers found that sleep deprivation in mice triggers both electrophysiological changes in brain activity and molecular stress responses, including endoplasmic reticulum stress and the unfolded protein response. However, when mice were exposed to flickering light stimulation during sleep deprivation, which induced brief periods of neuronal silence resembling sleep states, the molecular stress markers were prevented while sleep pressure signals (slow-wave activity) actually increased during subsequent recovery sleep. This demonstrates that the brain's electrical signatures of sleep need can be separated from the cellular stress responses typically associated with sleep loss.
Why it matters
This research suggests that specific patterns of brain activity during wakefulness, rather than simply time spent awake, may drive cellular stress responses associated with sleep deprivation. The findings could inform development of interventions that reduce harmful molecular consequences of sleep loss while maintaining cognitive function, with potential applications for shift workers or situations where adequate sleep is difficult to obtain.
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⚠️ Preprint – Noch nicht peer-reviewed
Dieser Artikel wurde noch nicht von unabhängigen Experten begutachtet. Die Ergebnisse sind vorläufig und sollten mit Vorsicht interpretiert werden.
Sleep deprivation (SD) triggers characteristic changes in the cortical electroencephalogram (EEG) during waking and sleep, as well as upregulating molecular signatures of neuronal activity, synaptic plasticity, and endoplasmic reticulum (ER) stress. This includes the induction of the unfolded protein response (UPR), the primary marker and adaptive mechanism of ER stress. Yet how cortical neuronal activity during SD contributes to the induction of these molecular signatures remains unknown. Here we investigate whether manipulating cortical activity during SD with a physiological stimulation paradigm (flickering light stimulation, FLS) affects the induction of the UPR. As expected, SD alone upregulated activity-dependent and UPR-related genes in cortex and led to increased EEG slow-wave activity (SWA) during subsequent NREM sleep, an electrophysiological signature of sleep need. Delivering FLS during SD, however, prevented the upregulation of activity- and UPR-related genes while inducing an additional increase in SWA during subsequent sleep. Further analysis of neuronal firing revealed that FLS induced brief neuronal silent (OFF) periods in awake animals during stimulation, thereby shifting cortical activity towards a brain state resembling sleep. These findings suggest that physiological manipulation of cortical activity during waking is sufficient to dissociate molecular signatures of ER stress from electrophysiological markers of sleep pressure. We propose that global sleep wake history and cortical network dynamics differentially regulate activity-dependent transcription and the accumulation of sleep pressure.